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The effect of strength training on endurance performance: a new form of cross training?
Hirofumi Tanaka and Thomas Swensen
Department of Exercise and Sport Sciences
Ithaca College
Ithaca NY 14850
and
Department of Kinesiology
University of Colorado
Boulder CO 80309-0354
Winter 1997
2
Summary
In accordance with the principals of training specificity, strength and endurance exercise induce distinct
muscular adaptations. Endurance training, for example, decreases the activity of the glycolytic enzymes, but
increases intramuscular substrate stores, the activity of the oxidative enzymes, and capillary and mitochondrial
density. In contrast, weight training reduces mitochondria density, while marginally impacting capillary density, the
activity of the metabolic enzymes, and intramuscular substrate stores other than glycogen, which increases
significantly. The training modalities do induce one common muscular adaptation: they transform type IIb
myofibers into IIa myofibers. This transformation is coupled with opposite changes in fiber size, and in general,
contractile properties. As a result of these distinct muscular adaptations, endurance training facilitates aerobic
processes, whereas weight training increases strength and anaerobic power. Some performance data do not fit this
paradigm, however, as they indicate that strength training or the addition of strength training to an endurance
exercise regimen, which includes running or cycling, increases short- or long-term work capacity in sedentary or
well-trained individuals during treadmill exercise or cycle ergometry. Additional data show that strength training
also improves the lactate threshold in untrained subjects during cycling. These improvements may be linked to
strength training’s ability to alter myofiber size and contractile properties, adaptations that may increase muscle
force production. In contrast, traditional dry-land weight training or combined swim and weight training does not
enhance performance in competitive swimmers, despite substantially increasing upper body strength. Combined
swim and swim specific in-water resistance training programs, however, increase a competitive swimmer’s velocity
in distances up to 200 m. This change is more closely associated with improved stroke mechanics than increased
strength, which suggests that stroke mechanics are a more crucial determinate for swim success. In all, traditional
weight training may be a valuable adjunct to the exercise programs followed by endurance runners or cyclists, but
not swimmers; these latter athletes need more specific forms of resistance training to realize performance gains.
3
Introduction
Traditional endurance training increases an athlete’s ability to perform low-resistance, high-repetition
exercise, but marginally impacts strength and anaerobic power. In contrast, weight training improves an athlete’s
ability to perform high-resistance, low-repetition exercise, but marginally affects endurance. It is inconsistent,
therefore, to prescribe strength training to an athlete who only wants to improve endurance, as such a prescription
violates the principles of training specificity, i.e., training programs should simulate the athlete’s mode of exercise
(McCafferty and Horvath 1977).
To perform well in most endurance sports, however, athletes need more than an enhanced long-term work
capacity; they also require strength and anaerobic power, abilities needed for climbing short steep hills, attacking,
and sprinting (Burke 1983, Bulbulian et al. 1986). To obtain proficiency at these skills, athletes typically perform
intense short intervals (Daniels and Scardina 1984), but many coaches and trainers have recently started to prescribe
strength training in conjunction with or in lieu of intervals, particularly in the off-season. This prescription is based
on weight training’s ability to improve strength and anaerobic power, and as result, possibly endurance
performance. In this capacity, weight training may be viewed as a form of cross-training, albeit a non-traditional
application of the concept. Traditionally, cross-training involves activities that produce a common goal, such as
improving V
.
O
2
max (Tanaka 94). Weight training fits this paradigm, but from a different perspective: as with short
intervals, it enhances anaerobic power. The body of scientific literature, however, is equivocal on strength
training’s impact on endurance performance.
Our purpose, therefore, is to examine the research on weight, endurance, and combined weight and
endurance training to understand the physiological basis for adding strength exercises to an endurance athlete’s
training regimen. To tighten our focus, we will concentrate only on the muscular adaptations induced by these
aforementioned training modalities. In the remaining sections of this review, we will examine strength training’s
impact on endurance run, cycle, and swim performance, the three forms of exercise traditionally integrated into a
cross-training regimen (Tanaka 1994)
4
Physiological Adaptations to Strength and Endurance Training
Strength training involves high load, low velocity muscular contractions, whereas endurance training
involves low load, high velocity muscular contractions. As a result of these differences, each training mode
produces distinct physiological adaptations in the trained musculature. Strength training, for example, induces
muscle hypertrophy as measured by increased cross-sectional area in all fiber types or just the fast twitch fibers
(Hather et al. 1991, Houston et al. 1983, Kraemer et al. 1995, MacDougall et al. 1979, MacDougall et al. 1980,
Ploutz et al. 1994, Staron et al. 1989, Staron et al. 1991, Tesch et al. 1987). This hypertrophy reflects an increase in
muscle protein content, resulting in increased fiber size and possibly number (Goldberg et al. 1975, Gonyea 1981,
Kraemer et al. 1996, MacDougall 1992). Strength training also alters the ratio of the fast twitch fibers, as IIa fiber
percentage increases and IIb fiber percentage decreases, a concomitant change reflecting a IIb to IIa fiber
transformation at a histochemical and myosin isoform level (Abernathy et al. 1994, Adams et al. 1993, Fitts and
Widrick 1996, Hather et al. 1991, Klitgaard et al. 1990, Kraemer et al. 1995, Kraemer et al. 1996, MacDougall et al.
1980, Ploutz et al. 1994, Staron et al. 1989, Staron et al. 1991, Staron et al. 1994).
In contrast to these structural changes, strength training has only a modest impact on the activity of the
metabolic enzymes. Short-term training programs (< 24 wk), for example, induce little to no change in the activity
of the phosphagen, glycolytic, or oxidative enzymes, including myokinase (MK), myosin ATPase, creatine kinase
(CK), hexokinase, lactate dehydrogenase (LDH), phosphofructokinase, succinate dehydrogenase (SDH), citrate
synthase, and 3-OH-acyl-co-A-dehydrogenase (Hickson et al. 1988, Houston et al. 1983, Nelson et al. 1990, Ploutz
et al. 1994, Tesch et al. 1987, Tesch et al. 1990, Thorstensson et al. 1976). Longer-term weight training programs
affect most of the aforementioned enzymes similarly, although the activity of LDH and MK in the fast twitch fibers
of highly trained athletes is higher when compared to sedentary controls (Tesch et al. 1989).
Similar to strength training’s impact on enzyme activity, its affect on muscle capillarization is also modest.
The data from most studies indicated that strength training induces capillary neoformation, or implied that
neoformation occurs because capillary density does not change despite muscle hypertrophy (Hather et al. 1991,
Lüthi et al. 1986, Schantz 1982). The data from another study, however, showed that strength training does not
induce capillary neoformation, as capillary density but not number decreases (Tesch et al. 1984). Note that even if
5
strength training induces capillary neoformation, it does not increase capillary density. At best, strength training
maintains capillary density, which suggests that the O
2
diffusion distance, and hence O
2
delivery, will remain at pre-
training levels.
Compared to strength training’s affect on capillarization, its impact on mitochondrial density is
pronounced, as the density of this key metabolic organelle decreases, primarily via hypertrophy induced dilution
(MacDougall et al. 1979, MacDougall et al. 1986, Lüthi et al. 1986). In contrast, strength training equivocally
impacts the levels of intramuscular phosphagen and ATP, as data from one study indicated that strength training
increases these variables, whereas data from another study showed that they did not change (MacDougall et al.
1977, Tesch et al. 1990). Strength training does, however, increase the glycogen content of the trained musculature
(MacDougall et al. 1977 and Tesch et al. 1986).
In all, the most germane adaptive response to strength training may be the increase in myofiber size, which
is linked to altered contractile properties (Fitts and Widrick 1996, Widrick et al. 1996 a and b). Collectively, these
adaptations may increase muscle force production, and hence, constitute the musculature’s contribution to the
changes associated with weight training, such as increased strength, Wingate performance, short-term power output,
and time to exhaustion at heavy submaximal workloads (Bryant et al. 1988, Duchateau and Hinuat 1995, Fitts and
Widrick 1996, Hickson et al. 1980, Hickson et al. 1988, Kraemer et al. 1995). Note that the increases in short-term
power output and time to exhaustion at heavy submaximal work loads were not associated with significant changes
in V
.
O
2
max. Indeed, when all forms of weight training are considered together, this training modality increases
V
.
O
2
max by less than 3%, and then only in untrained or moderately active individuals (Allen et al. 1976, Gettman et
al. 1978, Gettman et al. 1979, Gettman and Pollock 1981, Gettman et al. 1982, Hickson 1980, Hickson et al. 1980,
Hickson et al. 1988, Hunter et al. 1987, Hurley et al. 1984, Kraemer et al. 1995, Nelson et al. 1990, Wilmore et al.
1978).
In contrast to strength training, endurance exercise unequivocally increases capillary density, mitochondrial
density, the activity of the oxidative enzymes, and intramuscular substrate stores, while also reducing the activity of
the glycolytic enzymes (Dudley and Djamil 1985, Hickson et al. 1980, Hollozsy and Booth 1976, Hollozsy and
Coyle 1984, Klausen et al. 1981, Sale et al. 1990, Saltin and Gollnick 1983). As with strength training, endurance
exercise also alters the size and ratio of the fast twitch fibers, as it decreases their cross-sectional area, while
6
increasing IIa and decreasing IIb fiber percentages, a concomitant change reflecting a fiber transformation at a
histochemical and myosin isoform level (Fitts et al. 1989, Fitts and Widrick 1996, Jansson and Kaijser 1977,
Kraemer et al. 1995, Simoneau et al. 1985, Staron and Johnson 1993, Tesch and Karlsson 1985).
Endurance training’s impact on type I fiber percentage and size, however, is minimal when compared to
the type II fibers, as most data indicate that this training modality does not alter type I fiber percentage and reduces
or does not change type I fiber size (Widrick et al. 1996 a and b, Kraemer et al. 1995, Howald et al. 1985, Fitts et al.
1989, Gollnick et al. 1973). The fiber size data, moreover, are supported by cross-sectional studies and research on
rodents (Baldwin et al. 1972, Fitts and Widrick 96, Jansson and Kaijser 1977, Tesch et al. 1985). The data from
several other papers, in contrast, showed that endurance training induces type I fiber hypertrophy (Simoneau et al.
1985, Gollnick et al. 1973). A possible source for some of the discrepancy in the type I fiber size data may be the
pre-training fitness level of the subjects, as fiber size increased in untrained individuals and decreased or did not
change in moderately to highly trained athletes. Alternatively, these data suggest that the acute response to
endurance training is type I fiber hypertrophy, whereas the chronic response is atrophy.
Aside from altering fiber size and percentage, endurance training also affects the contractile properties of
the myofibers, as it lowers the maximum shortening velocity (V
.
max
)
of the type II fibers and slightly reduces peak
tension development in all fiber types (Fitts and Widrick 1996, Fitts et al. 1985, Fitts et al. 1977, Fitts et al. 1982,
Schluter and Fitts 1994). Collectively, the changes in myofiber size and contractile properties lower the maximum
force generating capability of the type I and IIa fibers (Fitts and Widrick, Widrick et al. 1996a and b). The decrease
in force production, especially in the IIa fibers, is not necessarily deleterious to endurance performance, as it may be
linked to increased fiber efficiency (Fitzsimons et al. 1990, Fitts and Widrick 1996). A smaller, more efficient IIa
fiber may be advantageous for endurance exercise, as increased fiber efficiency would reduce the rate of ATP
utilization, and decreased fiber diameter would enhance O
2
delivery by shortening the O
2
diffusion distance. Both
changes could increase long-term work capacity.
Endurance training also increases the expression of fast myosin light chains in the type I fibers, which
increases their V
.
max
, shifting it towards a velocity more characteristic of the type IIa fibers (Fitts and Widrick 1996,
Schluter and Fitts 1994, Widrick et al. 1996 a). This adaptation does not, however, indicate a type I—type II fiber
transformation; such a change requires altered myosin heavy chain expression, which has not been reported (Fitts
7
and Widrick 1996, Staron and Johnson 1993). An increased V
.
max
in the type I fibers may enhance muscle speed,
and hence body speed, without affecting fiber efficiency (Fitts and Widrick 1996, Widrick et al 1996 a). These
changes may allow endurance athletes to reduce their use of the less efficient type II fibers at a given absolute
submaximal work load, which could account for the improved running economy induced by endurance exercise
(Morgan et al. 1995).
Collectively, the aforementioned muscular adaptations induced by endurance training facilitate aerobic
processes, as this training modality increases V
.
O
2
max, lactate threshold, and long-term work capacity. In contrast,
these muscular adaptations, especially the changes in myofiber size, percentage, and contractile properties, may
compromise anaerobic power and strength, as endurance training reduces Wingate anaerobic power, vertical leap,
and leg strength (Costill et al. 1967, Fitts and Widrick 1996, Jones and McCartney 1986, Kraemer et al. 1995, Ono
et al. 1976).
Resistance and endurance training, therefore, induce one common muscular adaptation: they transform IIb
fibers into IIa fibers. This transformation is coupled with opposite changes in fiber size, and in general, contractile
properties, which may explain why weight but not long distance exercise improves anaerobic power and strength.
From the perspective of affecting those variables traditional associated with enhanced endurance, such as capillary
density, mitochondrial density, or the activity of the oxidative enzymes, strength and endurance training are not
synergistic.
Simultaneous Training for Strength and Endurance
The interaction between resistance and endurance training in untrained subjects was first studied by
Hickson (1980). He reported that concurrent resistance and endurance exercise induces a similar increase in V
.
O
2
max as endurance training, but attenuates strength gains when compared to weight training. Hickson speculated
that the training load may have caused the attenuated strength gain, as the concurrently trained group performed
both exercise modalities each week day and completed additional endurance training on the weekend, whereas the
resistance trained group performed only strength exercises five days a week. The data from subsequent studies in
which the training load was reduced, however, confirm that concurrent training in sedentary individuals attenuates
gains in strength when compared to resistance training (Hunter et al 1987, Dudley and Djamil 1985). Although the
8
mechanism for this antagonism is unresolved, the data from a recent concurrent training study in which active
soldiers served as subjects (Kraemer et al. 1995) suggest that differential changes in fiber size might contribute to
the attenuation of strength induced by this training modality.
In this study, resistance training increased the size of all fiber types, while increasing IIa and decreasing IIb
fiber percentages, reflective of a IIb to IIa fiber transformation. Concurrent training, in contrast, marginally reduced
the size of the type I, IIc, and IIb fibers. Additionally, it may have also decreased the size of the type IIa fibers
despite a measured increase in their cross-sectional area; this change probably indicates a IIb to IIa fiber
transformation rather than IIa fiber hypertrophy, as this training modality increased IIa and decreased IIb fiber
percentages. Collectively these data show that endurance training in active soldiers, even with strength training
superimposed, tends to promote smaller muscle fibers than only strength training. As discussed earlier, smaller
muscle fibers and the associated changes in fiber contractile properties induced by endurance training (decreased V
.
max
in the type II fibers, increased V
.
max
in the type I fibers, and reduced peak tension development in all fibers) may
facilitate aerobic processes, while compromising anaerobic power and strength. Indeed, the concurrently trained
group in this study had a statistically similar increase in V
.
O
2
max as the endurance trained group, but an attenuated
gain in leg strength and Wingate anaerobic power when compared to the resistance trained group. The data from
the endurance trained group further support our argument, as this group experienced the largest percentage increase
in
V
.
O
2
max and the largest percentage decrease in fiber size; the latter change, moreover, was associated with 1.2%
reductions in leg strength and Wingate anaerobic power.
The attenuation of strength gains in sedentary or moderately active individuals after concurrent training
may also be due to a time course interaction, i.e., the body cannot adapt maximally to both training stimuli if they
are initiated simultaneously. This line of reasoning is supported by data that show well-trained endurance athletes
do not experience attenuated strength gains when they add resistance exercises to their endurance training regimen
(Hunter et al. 1987). Additional support for this hypothesis is provided by data collected from research on rodents,
which indicate that hypertrophying muscle experiences attenuated gains in endurance, whereas previously
hypertrophied muscle responds similarly to endurance training as untrained muscle (Stone et al. 1996, Riedy et al.
1985).
9
Effects of Strength Training on Endurance
a) Effects of strength training on endurance run performance:
Few studies have examined resistance training’s impact on endurance run performance. Improvements in
strength and anaerobic power acquired through weight training could, however, help runners sustain attacks, climb
hills, or sprint, which should enhance performance. Indeed, data show that anaerobic power is a critical determinate
for race success in aerobically homogeneous cross-country runners and that the fastest 10 km runners possess the
most powerful muscles (Bulbulian et al. 1986, Noakes 1988).
The first studies to examine weight training’s affects on run performance used untrained subjects, which
limits our ability to extend the findings to highly trained athletes. Nevertheless, these studies showed that weight
training improves short-term treadmill performance by 10% and leg strength by 27% (Gettman et al. 1978, Gettman
et al. 1979, Gettman et al. 1982, Hickson et al. 1980, Wilmore et al. 1978). The change in V
.
O
2
max in these studies
depended on the strength training stimulus, as heavy resistance weight training did not affect this variable, whereas
circuit weight training improved it by 6%. Recall, however, that when all forms of weight training are considered
together, this training modality increases V
.
O
2
max by less than 3%, and then only in sedentary or moderately active
individuals.
As with untrained subjects, weight training also improves short-term treadmill performance, leg strength,
and anaerobic power in moderately trained endurance athletes. Data from one study, for example, indicated that the
addition of strength exercises to an endurance training regimen improves short-term treadmill performance by 13%
and leg strength by 30% (Hickson et al. 1988). Similarly, data from another study showed that weight training
increases leg strength by 40% and vertical leap by 15% in previously trained runners, indicating enhanced anaerobic
power, and hence, possibly run performance (Hunter et al. 1987). Neither study found that strength training altered
V
.
O
2
max in endurance trained individuals.
The underlying muscular adaptations responsible for the improved short-term run performance in either
sedentary or trained individuals are unknown. Since weight lifting decreases mitochondrial density and minimally
impactsV
.
O
2
max, capillary density, substrate stores, and the activity of the metabolic enzymes, the keys may be the
increase in myofiber size and the associated changes in contractile properties induced by this training modality.
10
Although the effect of weight training on myofiber size in highly trained runners has not been studied, concurrent
training in active soldiers produces larger myofibers and greater gains in strength and Wingate performance then
endurance exercise (Kraemer et al. 1995). In short, if weight training can induce fiber hypertrophy in a fit runner,
then it may alter some of the muscular changes produced by endurance exercise. For example, increased fiber size
may further improve slow twitch fiber V
.
max
while attenuating or reversing the reduction in the V
.
max
of the fast twitch
fibers and peak tension development in all fibers (Fitts and Widrick 1996, Fitts et al. 1977, Fitts et al. 1982, Fitts et
al. 1989, Schluter and Fitts 1994, Widrick et al. 1996a and b). Since faster, larger, and stronger fibers generate
more force, weight trained runners may be able to exercise longer at each absolute submaximal work load by
reducing the force contribution from each active myofiber or by using fewer of them. In conjunction, a stronger
type I fiber may allow weight trained runners to delay the recruitment of the less efficient type II fibers, as
previously suggested (Hickson et al. 1988, 1980).
Our hypothesis is indirectly supported by data that show weight training reduces the integrated
EMG/muscle tension ratio at absolute submaximal work loads in untrained subjects (Komi et al. 1978, Moritani and
deVries 1979, Moritani and deVries 1980). These data can be interpreted in at least two ways: they may indicate
that the degree of activation per motor unit/muscle fiber is lower or that fewer motor units/muscle fibers are active
(Basmajian and De Luca 1985). Based on the motor unit size principle, moreover, this latter alternative implies that
large motor unit activity is reduced, i.e., fewer, less efficient fast twitch fibers are active. Additional support for our
hypothesis is provided by data that show weight training improves running economy in fit runners (Johnston et al.
1995). Running economy is partially related to type I fiber percentage or V
.
max
or both factors (Coyle (1995). Since
weight training does not increase type I fiber percentage, it may improve running economy by augmenting the
increased V
.
max
seen in these fibers after endurance training.
b) Effects of strength training on endurance cycling performance
As with running, weight training may also improve endurance cycling performance, as dynamic strength is
an essential component of those facets of competitive road cycling requiring anaerobic and short-term power, such
as attacking, responding to an attack, climbing a short steep hill, or sprinting (Burke 1983). Indeed, the more highly
rated cyclists within the United States Cycling Federation, the governing body for amateur cycling in America, had
11
significantly higher anaerobic power outputs than the lower rated cyclists (Tanka et al. 1993). None of the work
that has examined weight training’s impact on cycling, however, has used highly trained cyclists as subjects, so it is
uncertain if the results apply to this population. Nonetheless, the data indicate strength training may improve
certain aspects of cycling performance.
Data from the studies that examined strength training’s impact on cycling specific anaerobic power, for
instance, showed that this training modality increases Wingate performance (range: 6% to 17%) and leg strength
(range: 3% to 30%) in sedentary individuals, active soldiers, and elite swimmers (Inbar et al. 1981, Kraemer et al.
1995, Petersen et al. 1984). Additional data showed that weight training improves short-term cycling performance
by 29% and leg strength by 35% in untrained subjects (Bryant et al. 1988, Hickson et al. 1980). Data from a
subsequent study indicated that the addition of weight training to a well trained endurance athlete’s exercise
program also improves short-term cycling performance by 11% and leg strength by 30% (Hickson et al. 1988).
Note that this training program also increased long-term cycling capacity by 20%, as measured by time to
exhaustion at 80% of V
.
O
2
peak. This finding is supported by data that shows weight training increases time to
exhaustion at 75% of
V
.
O
2
peak by 33% in untrained subjects (Marcinik et al. 1991). The mean change in absolute V
.
O
2
peak in the
aforementioned studies reporting data on this variable was 2% (Hickson et al. 1980, Hickson et al. 1988, Kraemer et
al. 1995, Marcinik et al. 1991).
The muscular adaptations responsible for the increases in anaerobic power and short- or long-term work
capacity are unknown. From a gross perspective, the gains in anaerobic power correlate well to the increases in leg
strength (Inbar et al. 1981, Rutherford 1986, Smith 1987). From a cellular perspective, we refer you to the
hypothesis elucidated in the previous section on running: namely, the changes in fiber size, percentage, and
contractile properties induced by weight training may allow the subjects to exercise longer at a given absolute
submaximal work load by reducing the force contribution from each active myofiber or by using fewer of them. In
conjunction, the myofiber changes may also allow the subjects to delay the recruitment of the less efficient type II
fibers.
Additional support for our hypothesis is found in the study by Marcinik et al. (1991), whose data indicated
that the 33% increase in long-term cycling capacity induced by weight training was associated with a 12% increase
12
in the lactate threshold. Indeed, their subjects’ mean blood lactate was 30% lower at the same absolute submaximal
work load after training. These data reflect a lower overall activation of the working musculature, and hence, its
mitochondria. As a result, disturbance of cellular homeostasis would be reduced, as would glycogenolysis and
lactate production (Coyle 1995). Additional research is needed to determine if weight training can alter cycling
economy or glycogen depletion in the various types of myofibers, as such data would allow us to discern if fiber
recruitment patterns change.
c) Effects of strength training on endurance swim performance:
As with run and cycle endurance performance, dynamic strength is also an important determinate of swim
performance. Many studies have reported that upper-body strength and power correlate highly with swim times
over distances ranging from 23 m to 400 m, with an average r value of .87 for the shorter distance and .63 for the
longer distance (Costill et al. 1980, Davis 1959, Hawley and Williams 1990, Miyashita and Kanehisa 1979, and
Sharp et al. 1982, Toussaint and Vervoorn 1990). Even though the relationship between strength/power and swim
performance weakens as distance increases, it remains significant, which implies that weight training, through its
ability to increase strength and anaerobic power, may improve endurance swim performance.
Similar to running and cycling, the early studies that examined weight training’s impact on swim
performance used untrained subjects, which limits our ability to apply these results to highly trained individuals.
Nonetheless, data from these studies indicated that traditional weight training (e.g., barbells, universal machines,
etc.) or combined swim and weight training improves swim performance over a range of distances from 23 m to the
number of laps covered in 15 min (Davis 1955, Jensen 1963, Nunney 1960, Thompson and Stull 1959). The
improvements, however, were less than the gains induced by standard swim training with one exception, as data
from two of the studies showed that combined training produced marginally faster swim times over 30 m than swim
training (Jensen 1963, Nunney 1960). Collectively, these data suggest that combined swim and traditional weight
training may improve sprint but not endurance swim performance.
Tanaka et al. (1993) recently examined the effects of combined swim and traditional weight training on
sprint velocity in competitive college swimmers. Their data showed that combined training did not produce faster
sprint times than swim training, despite increasing upper-body strength by 31%. The authors speculated that the
13
strength gain induced by the weight training program did not translate into better performance because the swim
stoke is highly technical, i.e., traditional weight training is not specific enough to improve swim performance. This
hypothesis is supported by data that show combined swim and swim specific resistance training improves
performance more than swim or combined swim and traditional weight training in competitive swimmers (Kiselev
1991, Toussaint and Vervoorn 1990). In these studies, swim specific resistance exercise included: swim-bench
training, a form of dry-land specific weight training; reverse current hydrochannel swimming; and in-water devices
that the athletes push-off from while swimming. Additional data showed that in-water resistance training or swim
training in well conditioned children and recreational swimmers is more beneficial than dry-land specific weight
training (Bulgakova et al. 1990, Gergley et al. 1984).
The data from the aforementioned studies indicate that traditional weight training or combined swim and
weight training does not improve endurance performance in competitive swimmers. In contrast, combined swim
and swim specific resistance training, particularly if executed in-water, improves a competitive swimmer’s velocity
in distances up to 200 m (Toussaint and Vervoorn 1990). The effects of combined swim and in-water resistance
training on performance over longer distances is unknown. We cautiously advance our interpretation of the data,
however, as several of the studies did not include a swim only control group (Bulgakova et al. 1990, Kiselev 1991).
Note that traditional and swim specific dry-land weight training induced greater gains in upper-strength than in-
water resistance training, whereas the latter training modality more favorably impacted those factors associated with
improved stroke mechanics, such as stroke force, number, and time (Bulgakova et al. 1990, Tanaka et al. 1993,
Toussaint and Vervoorn 1990). These data support the contention that stoke mechanics are an important
determinate for swim success, and imply that they are more crucial than upper body strength (Bulgakova et al. 1990,
Craig et al. 1979, Craig et al. 1985, Costill et al. 1985, Tanaka et al. 1993, Toussaint and Vervoorn 1990).
Conclusion:
Traditional weight training may be a valuable adjunct to the exercise programs followed by runners and cyclists, as
it improves anaerobic power, and short- and long-term work capacity in sedentary or well trained athletes during
treadmill exercise or cycle ergometry. Whether strength training improves performance in elite cyclists or runners
is unknown. Nonetheless, the data suggest that strength training may be useful as a form of cross training for these
14
athletes, particularly in the off-season when they require a respite from their normal exercise modality, while also
needing to maintain as much strength, power, and work capacity as possible. The benefit of year round weight
exercises is an unresolved issue that cannot be addressed until we compare strength training to sport specific
interval training. In contrast, traditional weight training or combined swim and weight training does not improve
endurance performance in untrained or competitive swimmers, perhaps because it does not induce sufficient
improvement in stoke mechanics to increase swim velocity. Combined swim and in-water resistance training,
however, increases a competitive swimmer’s velocity over various distances during the season, which implies that
this type of resistance training is a valuable form of cross-training year round.
Acknowledgments
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